Plasma DBH activity has been suggested as a useful clinical index of sympathetic activity since, in some reports, it was shown to be elevated in persons with labile pressure, both normotensives and hypertensives. On the other hand, some work indicates that plasma DBH activity does not reflect plasma catecholamines (CA) levels nor does it change in response to short-acting sympathetic stimuli. To date, the only way to elevate plasma DBH in animals was by imposition of a secondary stress. The spontaneously hypertensive rat, often considered a suitable model of essential hypertension, has normal serum DBH and other common models of experimental hypertension apparently do not have elevated plasma DBH. My laboratory recently reported that plasma DBH activity is consistently elevated in the rat with neurogenic hypertension induced by sinoaortic denervation, SAD. Thus, we can study an animal model with high plasma DBH activity in conjunction with elevated arterial pressure. The objectives are to determine if plasma total CA and plasma norepinephrine (NE) are also increased in the SAD rat, and if they vary concordantly with plasma DBH. The relationship of plasma CA, NE and DBH activity to short-term blood pressure variations and to the duration of hypertension will be studied. The assay methods to be used for these plasma indices are among the most sensitive and specific ones available. A further objective is to determine if DBH contained in adrenal glands, mesenteric vessels and/or heart contributes to the elevated plasma DBH activity in SAD rats. The SAD model is uniquely suited for testing the combined effect of increased dietary sodium and high sympathetic activity on the course of blood pressure. This is unknown, to date, and will be studied along with the effect of high sodium intake on plasma DBH activity and CA.